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T Cell Conditioning Explains Early Disappearance of the Memory CD8 T Cell Response to Infection¹

Ali Jabbari^*, Kevin L. Legge^*, and John T. Harty^2,*,

^* Interdisciplinary Graduate Program in Immunology, Roy J. and Lucille A. Carver College of Medicine, University of Iowa, Iowa City, IA 52242; Department of Pathology, Roy J. and Lucille A. Carver College of Medicine, University of Iowa, Iowa City, IA 52242; and Department of Microbiology, Roy J. and Lucille A. Carver College of Medicine, University of Iowa, Iowa City, IA 52242

Memory CD8 T cells respond more rapidly to acute intracellular infections than naive CD8 T cells. An understanding of the biological processes involved in memory CD8 T cell recognition of Ag and up-regulation of effector mechanism necessitates analyzing memory CD8 T cells at early time points after infection. In the current study, we show that memory CD8 T cells ostensibly disappear from the spleens, blood, and peripheral organs of mice early after infection with Listeria monocytogenes. This disappearance is critically dependent on Ag, and cell-associated Ag alone can mediate this phenomenon. Further investigations, however, suggest that this disappearance is secondary to T cell-APC interactions, also known as T cell conditioning, and disruption of these putative interactions during splenic processing improves recovery of Ag-specific memory CD8 T cell populations after immunization. Conventional analyses of memory CD8 T cell populations early after infection and possibly in the presence of low levels of Ag (as during chronic infections) may exclude significant numbers of the responding CD8 T cell population.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This work was supported by National Institutes of Health Grants AI42767, AI46653, AI50073, and AI059752 (to J.T.H.) and by American Heart Association Heartland Predoctoral Grant 0610047Z (to A.J.).

² Address correspondence and reprint requests to Dr. John T. Harty, Department of Microbiology, University of Iowa, 3-512 Bowen Science Building, 51 Newton Road, Iowa City, IA 52242. E-mail address: john-harty{at}uiowa.edu

³ Abbreviations used in this paper: Tg, transgenic; LM-OVA, L. monocytgenes expressing the OVA gene; actA^– LM-ova, the attenuated strain of LM-OVA; DC, dendritic cell.

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